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Am J Physiol Lung Cell Mol Physiol 283: L1247-L1254, 2002. First published August 9, 2002; doi:10.1152/ajplung.00036.2002
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Vol. 283, Issue 6, L1247-L1254, December 2002

Modulation of endotoxin-induced NF-kappa B activation in lung and liver through TNF type 1 and IL-1 receptors

M. Audrey Koay1, John W. Christman1,3, L. James Wudel2, Tara Allos2, Dong-Sheng Cheng1, William C. Chapman2, and Timothy S. Blackwell1,3

Departments of 1 Medicine and 2 Surgery, Vanderbilt University School of Medicine, Nashville 37232-2650; and 3 Department of Veterans Affairs Medical Center, Nashville, Tennessee 37203

We investigated the requirement for tumor necrosis factor-alpha (TNF-alpha ) and interleukin (IL)-1 receptors in the pathogenesis of the pulmonary and hepatic responses to Escherichia coli lipopolysaccharide (LPS) by studying wild-type mice and mice deficient in TNF type 1 receptor [TNFR1 knockout (KO)] or both TNF type 1 and IL-1 receptors (TNFR1/IL-1R KO). In lung tissue, NF-kappa B activation was similar among the groups after exposure to aerosolized LPS. After intraperitoneal injection of LPS, NF-kappa B activation in liver was attenuated in TNFR1 KO mice and further diminished in TNFR1/IL-1R KO mice; however, in lung tissue, no impairment in NF-kappa B activation was found in TNFR1 KO mice and only a modest decrease was found in TNFR1/IL-1R KO mice. Lung concentrations of KC and macrophage-inflammatory peptide 2 were lower in TNFR1 KO and TNFR1/IL-1R KO mice after aerosolized and intraperitoneal LPS. We conclude that LPS-induced NF-kappa B activation in liver is mediated through TNF-alpha - and IL-1 receptor-dependent pathways, but, in the lung, LPS-induced NF-kappa B activation is largely independent of these receptors.

sepsis; macrophage; neutrophil; cytokines; chemokines


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